01-03 Intro to FEK Flashcards

1
Q

Intracellular vs. Extracellular Enviro
—% TBW
—subdivided?
—[electrolytes]

A

INTRA
—2/3 TBW
—not subdivided
—high [K+] (~150mEq) and low [Na+] (~10mEq) maintained by Na+/K+-ATPase

EXTRA
—1/3 TWB
—subdivided: 1/4 intravasc, 3/4 interstitial
—low [K+] (~4mEq) and high [Na+] (~140mEq)

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2
Q

Average fluid osmolality in body

A

~285-295mOsm/kg

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3
Q

If you give 1200cc free water, how will it distribute?

A

800cc into cells (intracelluar = 2/3)
300cc to interstitium (extracelluar-interstitial = 2/13)
only 100cc stays in vasculature! (extracellular-intravasc = 1/12)

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4
Q

If you give 1200cc normal saline, how will it distribute?

A

Because of Na+, almost none into cells so:
—900 (3/4) goes to interstitial
—300 (1/4) stays in vasculature

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5
Q

If you give 1200cc KCl sol’n, how will it distribute?

A

You just killed your pt.

—all to cells assuming isotonic (300mOsm/kg)

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6
Q

If you give 1200cc half-normal (0.45%) saline, how will it distribute?

A

Half as much stays in vasculature:
—200cc (1/6) stays in vasculature
—1000 (5/6) to interstitium/cells
like giving 600cc NS and 600cc free H2O: do it out

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7
Q

creatinine handling by (healthy) kidney

A

—~90% freely filtered; ~10% secreted

—NOT reabsorbed, thus analogue for GFR

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8
Q

normal GFR

A

women: 130-145L/d
men: 165-180L/d

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9
Q

endocrine fxns of kidney

A
  • epo
  • renin, A-II, prostaglandins
  • calcitriol synth
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10
Q

PT

A

—50-90% of filtered substances absorbed here
—uptake usu. coupled to Na+ via COTRANSPORTERS
——1/2 to 2/3 Na+
——90% HCO3-
——~all glucose/a.a.’s
—urine leaves isotonic

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11
Q

LoH

A
—Na+/K+/2Cl- pump (loop diuretics block)
—descending limb: H2O perm
—ascending limb: H2O IMperm
—countercurrent mech:
1. filtrate comes in with higher [Na+]
2. descends losing water (but not Na+!) to hypertonic medulla concentrating the urine
3. ascends losing Na+ (but not water!) into increasingly hypotonic medulla
4. leaves with more dilute urine
5. final urine [H2O] determined in CT
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12
Q

DT

A

—Na+/Cl- co-transporter (blocked by thiazides)
—major site of Ca2+ reabsorption

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13
Q

CD

A

—site of ADH & ANP action (opposite effects on Na+ channel)
—major K+ reg site
—Cl- via tight jct in between cells b/c of lumen q- caused by Na+ pumping out of lumen
—principal cells: resorb Na+ & H2O/secrete K+ aldosterone-dependent (site of spironolactone action)
—intercalated cells: maintain acid/base balance

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14
Q

effect of thiazides of serum [Ca2+]

A

they cause hypercalcemia [see image]

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15
Q

What hormones does the kidney produce?

A

—renin
—epo
—calcitriol

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16
Q

Which hormones act on the kidney?

A
—A-II
—alodsterone
—ANP
—ADH
—PTH
—calcitriol

(epi?)

17
Q

True or False: Na+ reabsorption is stimulated by hyponatremia?

A

FALSE
—Na+ reuptake is stiumulated by the R-A-A-S system which is activated by: 1) low tubular flow and 2) low pressure at baroreceptors

18
Q

Major regulator of [K+]

A

aldosterone

—stimulates Na+ reabsorption and K+ secretion

19
Q

Effect of tubular flow on K?

A

high tubular flow (as with polyuria) —> creates gradiant favorable for K+ secretion

20
Q

Major regulators of [H+]

A

pH sensors cause release of:
—Aldosterone: stimulates H+ secretion (?)
—A-II: stimulates bicarb reabsorption (alkalosis)
[H+] also varies w/ ∆ing K+

21
Q

Main sites and actors of water regulation in kidney

A

Hypothal osmoreceptors sense ↑ osmolality (i.e. not volume) → ADH release
—low [Na+] doesn’t ↑ Na+ reabsorption but it DOES increase H2O wasting
***This is overridden in cases of significant hypovolemia where ADH takes on its “vasopressin” role and hangs onto water even in the face of hyponatremia
—ADH is regulating hormone
—H2O reabsorbed in the descending LoH
—H2O excreted in distal tubule which is water-impermeable but reabsorbs NaCl

22
Q

Body adjusts ______ to ∆ osmolality

Body adjusts ______ to ∆ volume

A

Body adjusts amount of WATER to ∆ osmolality

Body adjusts amount of SODIUM to ∆ volume

23
Q

Pt goes into renal failure s/p ACEI Rx. What do they have?

A

classically, R.A.S.
—in R.A.S., glomeruli receive so little RBF they clamp down their EAs to maintain filtration pressure
—ACEI caused dilation of the efferent arteriole causing plummeting GFR

24
Q

Triad for nephrotic syndrome

A
Proteinuria
edema
hypoalbuminemia
—qqf: hyperlipidemai
—qqf: lipiduria
usually non-inflamm
25
Q

Glomerulonephritis

A

hematuria!
—often renal schistocytes b/c RBCs damaged going through GBM
—RBC casts = nephritic syndrome

proteinuria often present, too, but less than w/ nephrotic syndrome